Peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS), is an aggressive mature T-cell neoplasm that may present with nonspecific systemic and metabolic abnormalities. A 73-year-old man with type 2 diabetes mellitus presented with progressive weakness, altered mental status, recurrent hypoglycemia, and hypercalcemia, accompanied by acute kidney injury, pancytopenia, diffuse lymphadenopathy, and splenomegaly. A complete critical-sample evaluation during hypoglycemia was unavailable, and the mechanism of the parathyroid hormone (PTH)-independent hypercalcemia could not be established because PTH-related peptide and vitamin D metabolite measurements were unavailable. Core biopsy of a left axillary lymph node demonstrated a mature CD4-positive T-cell lymphoma with strong diffuse CD30 expression, reduced CD7, negative anaplastic lymphoma kinase and Epstein-Barr virus-encoded RNA studies, and a Ki-67 proliferation index exceeding 90%, supporting PTCL-NOS after exclusion of other supported mature T-cell lymphoma entities. Classification remained limited by the absence of an excisional biopsy and additional molecular studies. Prednisone cytoreduction was followed by cyclophosphamide, doxorubicin, and prednisone, with brentuximab vedotin planned but not documented as administered. The course was complicated by profound myelosuppression, Klebsiella pneumoniae pneumonia, and neutropenic septic shock. Formal response assessment was not possible because complete staging and adequate follow-up were unavailable. This case highlights the importance of prompt tissue diagnosis when unexplained metabolic abnormalities coexist with cytopenias and generalized lymphadenopathy. Although hypoglycemia and hypercalcemia occurred in association with PTCL-NOS, the available data do not establish a causal or paraneoplastic relationship.

Calcium is essential for neuromuscular signaling, cardiovascular stability, and metabolic regulation. Disturbances in calcium homeostasis can exacerbate critical illness in small animal patients, whereas more profound abnormalities are associated with life-threatening complications. Although not frequently encountered, both hypocalcemia and hypercalcemia require rapid recognition and targeted therapy in an emergency setting. This article reviews the fundamental principles of calcium regulation, outlines the major etiologies and clinical features of disordered calcium balance, and provides an evidence-based approach to acute management. Practical considerations for monitoring, fluid and drug therapy, and supportive care are emphasized. Finally, we present novel and experimental interventions under evaluation in both veterinary and human medicine, highlighting areas in which future research may improve treatment options for animals.

Hypoparathyroidism(HypoPT) is rare, and real-world studies of biochemical control in affected patients are limited. This study aimed to analyze biochemical control in a large cohort of patients with adult-onset chronic HypoPT. Subjects were selected from outpatients followed at our center from June 2009 to March 2023. Proportion of measurements in/above/below the target range (MIR/MAR/MBR) and estimated time in/above/below the target range (TIR/TAR/TBR) were calculated. A total of 114 post-surgical (PS-HP) and 64 non-surgical (NS-HP) patients were enrolled, with a median follow-up of 82.5(45.0,108.0) months. The MIR/TIR were 70∼80% for serum calcium (Ca), around 40% for serum phosphorus(P), 80∼90% for 24-hour urine calcium(24hUCa), nearly 100% for calcium-phosphate products, 50∼64% for combined index 1(serum Ca and 24hUCa), and 20∼25% for combined index 2(all four indices). A total of 21 episodes of hypercalcemia occurred in 7 (3.93%) patients among the total 3455 measurements (0.61%). Compared to PS-HP patients, NS-HP patients showed poorer control of serum P, 24hUCa and combined indices. Serum Ca at diagnosis was positively associated with serum Ca TIR (β=21.15, P<0.05). Calcitriol dosage recorded at the last follow-up was negatively associated with TIR of serum Ca (β=-35.30, P<0.01) and 24hUCa (β = -66.19, P < 0.05). Hydrochlorothiazide use recorded at the last follow-up was associated with a 20.99% lower 24hUCa TIR (P < 0.001). Male patients showed higher serum P TIR than female (β1=28.14, P<0.001; β2=16.96, P<0.05). The control of serum Ca and 24hUCa was acceptable, whereas serum P and overall indices were suboptimal in our center. NS-HP patients showed poorer biochemical control than PS-HP patients and need more attention.

In patients with hypercalcemia and normal or mildly elevated parathyroid hormone (PTH) levels, distinguishing primary hyperparathyroidism (PHPT) from hypocalciuric hypercalcemia (HH) is crucial. We describe a 70-year-old woman who underwent parathyroidectomy for PHPT at 58 years old. Despite surgery, she remained asymptomatic with persistent hypercalcemia, normal phosphate levels, 25-hydroxyvitamin D, renal function, and mildly elevated PTH levels. Serial imaging suggested recurrent parathyroid disease, and subtotal parathyroidectomy demonstrated parathyroid hyperplasia. Although serum calcium and PTH levels initially normalized, hypercalcemia later recurred with normal PTH levels. Twenty-four-hour urinary calcium excretion was markedly low, and the calcium-to-creatinine clearance ratio (CCCR) was consistent with HH. No pathogenic variant was detected in the calcium-sensing receptor gene (CASR). At 84 years old, the patient remained asymptomatic. Long-term follow-up supported the diagnosis of HH despite negative CASR testing. This case underscores the importance of measuring 24-hour urinary calcium excretion and calculating the CCCR in patients with hypercalcemia, particularly in asymptomatic individuals, before considering parathyroid surgery.

Background: Long-term survival in sarcoidosis patients can be predicted by several clinical and laboratory parameters. Hypercalcemia serves as a predominant, negative prognostic factor. In the current study, we aimed to identify other patient characteristics influencing outcomes over a 10-year period. Methods: This was a retrospective analysis of hospitalized sarcoidosis patients in a large, tertiary medical center. Results: During a 10-year period between 2014 and 2024, data from 89 sarcoidosis patients was collected using MDClone data-mining software. Overall, 13 patients suffered from hypercalcemia (median, corrected for blood albumin: 10.3 mg/dL [9.9-10.5] vs. 9.5 [9.2-9.8], p < 0.001). Patients with hypercalcemia had higher rates of renal failure (30.8% vs. 3.9%, p = 0.008), lower platelet counts (median 153 K/mcl [113-170] vs. 230 [190.7-263.5], p < 0.001), lower hemoglobin concentrations (median 10.2 g/dL [10.0-11.3] vs. 12.5 [10.8-13.6], p < 0.01), higher urea blood levels (median 88 mg/dL [46-130] vs. 38.5 [30-47.2], p < 0.001), higher creatinine levels (median 1.48 mg/dL [1.31-1.6] vs. 0.9 [0.76-1.05], p < 0.001), and lower albumin (mean 3.07 g/dL ± 0.47 vs. 3.57 ± 0.56, p = 0.003). Hypercalcemia was associated with lower, post-discharge survival rates (median 4.8 years [2.6-7.3] vs. 7.9 [3.3-12.1], p = 0.045) and higher rates of 3-year, post-discharge mortality (30.8% vs. 7.9%, p = 0.036). Thrombocytopenia was present in six patients (6.7%); four (66.7%) died within three years, compared with six of 83 patients without thrombocytopenia (7.2%; p = 0.001). In univariate analysis, hypercalcemia and thrombocytopenia were both associated with a higher risk of mortality within 3 years (HR = 4.11, 95% CI 1.16-14.57, p = 0.029 and HR = 13.92, 95% CI 3.88-49.93, p < 0.001, respectively). However, in a multivariate analysis, only patient age and thrombocytopenia continued to be associated with a statistically significant higher risk of death (HR = 7.04, 95% CI 1.46-33.99, p = 0.015). Five of the six patients with thrombocytopenia (83.3%) were subsequently diagnosed with hematologic malignancy, months to years after thrombocytopenia was identified. Conclusions: Thrombocytopenia was associated with higher three-year mortality and may represent a clinical warning sign for occult or subsequently diagnosed hematologic malignancy in patients with sarcoidosis.

Primary hyperparathyroidism (PHPT) during pregnancy is a rare clinical entity associated with substantial maternal and fetal morbidity, particularly when complicated by severe hypercalcemia. We present the case of a 44-year-old multigravida at 27 + 5 weeks' gestation who presented with symptomatic, severe hypercalcemia (3.12 mmol/L), and acute kidney injury. Diagnostic evaluation confirmed bilateral parathyroid lesions. Due to high surgical risk and patient refusal of traditional parathyroidectomy, ultrasound-guided laser thermal ablation (LTA) of the dominant right inferior adenoma was performed. The procedure induced a rapid reduction in parathyroid hormone (PTH) concentrations and normalization of serum calcium levels, accompanied by a marked recovery of renal function. Subsequent genetic testing identified a pathogenic MEN1 mutation, confirming multiple endocrine neoplasia type 1. At 39 weeks of gestation, the patient delivered a healthy infant via elective cesarean section, with no evidence of neonatal hypocalcemia. This case demonstrates that LTA may serve as a safe, effective, and minimally invasive alternative for managing severe PHPT in pregnancy when conventional surgery is contraindicated or declined. To our knowledge, this represents the first reported application of LTA in this specific clinical scenario.

Paraneoplastic syndromes (PNS) represent uncommon but clinically significant manifestations of neuroendocrine neoplasms (NENs) arising from ectopic hormone secretion, aberrant peptide processing, cytokine-mediated effects, or immune-mediated mechanisms. Although NENs are intrinsically capable of producing bioactive substances leading to PNS, the true prevalence of PNS in NENs remains uncertain and is likely underestimated. Paraneoplastic manifestations may precede tumor diagnosis, represent the first indication of an otherwise occult neoplasm, or emerge during disease progression, thereby providing valuable diagnostic, prognostic, and therapeutic information. Endocrine PNS, including ectopic adrenocorticotrophic hormone secretion, carcinoid syndrome, paraneoplastic hypercalcemia, syndrome of inappropriate antidiuretic hormone secretion, hypoglycemia and ectopic acromegaly, account for the majority of cases, whereas neurological PNS are rarer and predominantly associated with high-grade neuroendocrine carcinomas (NECs). Recent advances in molecular biology have revealed the importance of neuroendocrine lineage plasticity, transcriptional dysregulation, epigenetic reprogramming, and abnormal prohormone processing in the pathogenesis of these syndromes. Concurrently, improvements in biochemical testing, functional imaging, liquid biopsy technologies, and molecular profiling have enhanced diagnostic accuracy and disease monitoring. Management requires a multidisciplinary approach combining syndrome-directed therapies with tumor-targeted interventions, including surgery, somatostatin analogs, peptide receptor radionuclide therapy, targeted agents, specific chemotherapy regimens and emerging immunotherapeutic strategies. Despite substantial progress, significant gaps remain regarding epidemiology, accurate biomarkers, prognostic significance, and optimal management. This review summarizes current knowledge on pathophysiology, clinical spectrum, diagnosis, prognostic implications, and treatment of PNS associated with gastroenteropancreatic and lung NENs, while highlighting future research priorities and unmet clinical needs.